Myelin oligodendrocyte glycoprotein immunoglobulin G-associated disease: An overview

Kazuo Fujihara, Douglas K. Sato, Ichiro Nakashima, Toshiyuki Takahashi, Kimihiko Kaneko, Ryo Ogawa, Tetsuya Akaishi, Yuki Matsumoto, Yoshiki Takai, Shuhei Nishiyama, Hiroshi Kuroda, Tatsuro Misu, Masashi Aoki

Research output: Contribution to journalReview articlepeer-review

12 Citations (Scopus)


Myelin oligodendrocyte glycoprotein (MOG) is localized at the outermost layer of the myelin sheath and is accessible for autoantibodies. Although experimental autoimmune encephalitis induced with MOG immunization has been studied for 30 years, the results of previous reports on MOG immunoglobulin G (IgG) detection with enzyme-linked immunosorbent assay and Western blot are confusing. However, after the development of human MOG-transfected cell-based assay to detect conformational-sensitive MOG-IgG, unique groups of patients have been found seropositive, and MOG-IgG-associated disease has become a hot topic in clinical neuroimmunology. Currently, the clinical spectrum of MOG-IgG-associated disease includes idiopathic optic neuritis, acute disseminated encephalomyelitis, encephalitides (brainstem and cerebral cortical), idiopathic myelitis, atypical multiple sclerosis, aquaporin-4 IgG-negative neuromyelitis optica spectrum disorders and others. MOG-IgG-associated disease occurs in both children and adults, and the female:male ratio is almost 1:1. Pleocytosis in the cerebrospinal fluids during acute exacerbation is often seen, but oligoclonal IgG bands are usually negative. T helper cell 17, B cells and neutrophil-related cytokines appear to be upregulated intrathecally. The pathology of acute lesions is characterized by active inflammation demyelination with deposition of immunoglobulins and complements. Just like aquaporin 4 IgG-positive neuromyelitis optica spectrum disorders, some disease-modifying drugs for multiple sclerosis seem to be inefficacious in MOG-IgG-associated disease, and chronic immunosuppression is required to prevent relapse, especially in patients persistently positive for MOG-IgG. Our understanding of this newly recognized disease remains insufficient, and the progress of research is much expected.

Original languageEnglish
Pages (from-to)48-55
Number of pages8
JournalClinical and Experimental Neuroimmunology
Publication statusPublished - 2018 Mar


  • demyelinating disease
  • myelin oligodendrocyte glycoprotein
  • myelin oligodendrocyte glycoprotein antibody
  • neuromyelitis optica spectrum disorders

ASJC Scopus subject areas

  • Neuroscience (miscellaneous)
  • Immunology
  • Immunology and Microbiology (miscellaneous)
  • Clinical Neurology


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